Annals of Gastroenterology 

About: Annals of Gastroenterology is an academic journal published by Hellenic Society of Gastroenterology. The journal publishes majorly in the area(s): Medicine & Inflammatory bowel disease. It has an ISSN identifier of 1108-7471. It is also open access. Over the lifetime, 1793 publications have been published receiving 18602 citations.

The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems

Abstract: The gut-brain axis (GBA) consists of bidirectional communication between the central and the enteric nervous system, linking emotional and cognitive centers of the brain with peripheral intestinal functions. Recent advances in research have described the importance of gut microbiota in influencing these interactions. This interaction between microbiota and GBA appears to be bidirectional, namely through signaling from gut-microbiota to brain and from brain to gut-microbiota by means of neural, endocrine, immune, and humoral links. In this review we summarize the available evidence supporting the existence of these interactions, as well as the possible pathophysiological mechanisms involved. Most of the data have been acquired using technical strategies consisting in germ-free animal models, probiotics, antibiotics, and infection studies. In clinical practice, evidence of microbiota-GBA interactions comes from the association of dysbiosis with central nervous disorders (i.e. autism, anxiety-depressive behaviors) and functional gastrointestinal disorders. In particular, irritable bowel syndrome can be considered an example of the disruption of these complex relationships, and a better understanding of these alterations might provide new targeted therapies.

The endoscopic diagnosis of early gastric cancer

Abstract: The aim of this article is to demonstrate the basic principles for the endoscopic diagnosis of early gastric cancer. The diagnostic process can be divided into two steps, detection and characterization. Detection requires good endoscopic technique, and thorough knowledge. With regard to technique, we should administer the optimum preparation to patients, including an antiperistaltic agent. Furthermore, in order to map the entire stomach we need to follow a standardized protocol, and we propose a systematic screening protocol for the stomach. With regard to knowledge, we should be able to identify high-risk background mucosa, and we should be aware of the indicators of a suspicious lesion. Chromoendoscopy and magnifying endoscopy are promising image-enhanced endoscopic techniques for characterization. The proposed criteria for a cancerous lesion are as follows: conventional endoscopic findings of 1) a well-demarcated lesion and 2) irregularity in color/surface pattern; vessel plus surface classification using magnifying endoscopy with narrow-band imaging findings of 1) irregular microvascular pattern with a demarcation line or 2) irregular microsurface pattern with a demarcation line. Conventional endoscopy and subsequent image-enhanced endoscopy can both contribute to the detection of early gastric cancer.

Pathology of nonalcoholic fatty liver disease

Abstract: Nonalcoholic fatty liver disease (NAFLD) may be the most common cause of chronic liver disease in Western countries, with an estimated prevalence of up to 24% in the general population. NAFLD is considered the hepatic manifestation of the metabolic syndrome and has been etiologically correlated with insulin resistance. The histopathological spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), with or without fibrosis, and cirrhosis. Liver biopsy is the “gold standard” for diagnosing NASH in a patient with clinical features of NAFLD, image detected steatosis and chronically elevated liver enzymes. This review discusses the histopathological findings of NAFLD in adults and children, including features representing resolution of NASH following treatment and features of prognostic information. Additionally, current systems of semiquantitative assessment in NAFLD and NASH are reviewed and the concurrence of NAFLD and NASH with other chronic liver diseases, mainly hepatitis C, is discussed. Key words: steatosis, steatohepatitis, nonalcoholic, liver, pathology

Systemic treatment-induced gastrointestinal toxicity: incidence, clinical presentation and management.

Abstract: The toxicity of cancer chemotherapy is among the most important factors limiting its use. Clear delineation and communication of benefits and risks is an essential component of treatment decisions. Gastrointestinal toxicity during chemotherapy is frequent and contributes to dose reductions, delays and cessation of cancer treatment. The development of intervention strategies that could eliminate an expected side effect of chemotherapy is vital. Physiologic changes that can increase the toxicity of chemotherapy are decreased stem cell reserves, decreased ability to repair cell damage, progressive loss of body protein, and accumulation of body fat. Symptoms only arise when physiological functions are altered. The gastrointestinal symptoms arising during cancer chemotherapy can often be cured if newly acquired, and if gastrointestinal physiological deficits are identified. Developing new chemotherapy regimens with similar efficacy but less toxicity should be a priority for future research.

Molecular genetics of colorectal cancer.

Abstract: Approximately 90% of colorectal cancer cases are sporadic without family history or genetic predisposition, while in less than 10% a causative genetic event has been identified. Historically, colorectal cancer classification was only based on clinical and pathological features. Many efforts have been made to discover the genetic and molecular features of colorectal cancer, and there is more and more evidence that these features determine the prognosis and response to (targeted) treatment. Colorectal cancer is a heterogeneous disease, with three known major molecular groups. The most common is the chromosomal instable group, characterized by an accumulation of mutations in specific oncogenes and tumor suppressor genes. The second is the microsatellite instable group, caused by dysfunction of DNA mismatch repair genes leading to genetic hypermutability. The CpG Island Methylation phenotype is the third group, distinguished by hypermethylation. Colorectal cancer subtyping has also been addressed using genome-wide gene expression profiling in large patient cohorts and recently several molecular classification systems have been proposed. In this review we would like to provide an up-to-date overview of the genetic aspects of colorectal cancer.